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      Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury

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          Abstract

          The outbreak of the 2019-nCoV infection began in December 2019 in Wuhan, Hubei province, and rapidly spread to many provinces in China as well as other countries. Here we report the epidemiological, clinical, laboratory, and radiological characteristics, as well as potential biomarkers for predicting disease severity in 2019-nCoV-infected patients in Shenzhen, China. All 12 cases of the 2019-nCoV-infected patients developed pneumonia and half of them developed acute respiratory distress syndrome (ARDS). The most common laboratory abnormalities were hypoalbuminemia, lymphopenia, decreased percentage of lymphocytes (LYM) and neutrophils (NEU), elevated C-reactive protein (CRP) and lactate dehydrogenase (LDH), and decreased CD8 count. The viral load of 2019-nCoV detected from patient respiratory tracts was positively linked to lung disease severity. ALB, LYM, LYM (%), LDH, NEU (%), and CRP were highly correlated to the acute lung injury. Age, viral load, lung injury score, and blood biochemistry indexes, albumin (ALB), CRP, LDH, LYM (%), LYM, and NEU (%), may be predictors of disease severity. Moreover, the Angiotensin II level in the plasma sample from 2019-nCoV infected patients was markedly elevated and linearly associated to viral load and lung injury. Our results suggest a number of potential diagnosis biomarkers and angiotensin receptor blocker (ARB) drugs for potential repurposing treatment of 2019-nCoV infection.

          Electronic Supplementary Material

          Supplementary material is available for this article at 10.1007/s11427-020-1643-8 and is accessible for authorized users.

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          Most cited references23

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          An expanded definition of the adult respiratory distress syndrome.

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            Is Open Access

            A Novel Coronavirus Genome Identified in a Cluster of Pneumonia Cases — Wuhan, China 2019−2020

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              Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome.

              There is currently no optimal treatment or effective drug for severe acute respiratory syndrome (SARS), because the immunopathologic mechanism is poorly understood. To explore the immune mechanism underlying the pathogenesis of SARS, we studied the expression profile of cytokines/chemokines in the blood and the immunopathology of the lung and lymphoid tissues. Fourteen cytokines/chemokines in the blood of 23 patients with SARS were dynamically screened, using a bead-based multiassay system. Reverse transcription-polymerase chain reaction was performed to amplify mRNA. Histopathology of the lung and lymphoid tissues at autopsy was examined, using methods of immunohistochemistry and double immunofluorescence staining. Interferon-inducible protein-10 (IP-10) was markedly elevated in the blood during the early stage of SARS, and remained at a high level until convalescence. Moreover, IP-10 was highly expressed in both lung and lymphoid tissues, where monocyte-macrophage infiltration and depletion of lymphocytes were observed. The levels of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 were concomitantly increased in the blood of the patients with superinfection, and the mRNAs for these cytokines were also increased in lung tissues. Induction of IP-10 is a critical event in the initiation of immune-mediated acute lung injury and lymphocyte apoptosis during the development of SARS. Superinfection after the immune injury is the main cause of death. The prompt elevation of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 is a sign of superinfection, indicating a high risk of death.
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                Author and article information

                Contributors
                yingxialiu@hotmail.com
                jiang@pumc.edu.cn
                liulei3322@aliyun.com
                Journal
                Sci China Life Sci
                Sci China Life Sci
                Science China. Life Sciences
                Science China Press (Beijing )
                1674-7305
                1869-1889
                9 February 2020
                2020
                : 63
                : 3
                : 364-374
                Affiliations
                [1 ]GRID grid.410741.7, Shenzhen Key Laboratory of Pathogen and Immunity, National Clinical Research Center for Infectious Disease, State Key Discipline of Infectious Disease, , Shenzhen Third People’s Hospital, Second Hospital Affiliated to Southern University of Science and Technology, ; Shenzhen, 518112 China
                [2 ]GRID grid.59053.3a, ISNI 0000000121679639, Hefei National Laboratory for Physical Sciences at the Microscale and School of Life Sciences, , University of Science and Technology of China, ; Hefei, 230027 China
                [3 ]GRID grid.12527.33, ISNI 0000 0001 0662 3178, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Biochemistry, , Peking Union Medical College, ; Beijing, 100005 China
                [4 ]GRID grid.9227.e, ISNI 0000000119573309, Institute of Microbiology, , Chinese Academy of Sciences, ; Beijing, 100101 China
                [5 ]GRID grid.413106.1, ISNI 0000 0000 9889 6335, Emergence Department Peking Union Medical College Hospital, ; Beijing, 100731 China
                Article
                1643
                10.1007/s11427-020-1643-8
                7088566
                32048163
                c5ce440f-d2fb-4613-a520-7238a3986755
                © Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature 2020

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                : 5 February 2020
                : 8 February 2020
                Categories
                Research Paper
                Custom metadata
                © Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature 2020

                2019-ncov,angiotensin ii,ards
                2019-ncov, angiotensin ii, ards

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